Abstract
This review paper delves into the current body of evidence, offering a thorough analysis of the impact of large-conductance Ca(2+)-activated K(+) (BK(Ca) or BK) channels on the electrical dynamics of the heart. Alterations in the activity of BK(Ca) channels, responsible for the generation of the overall magnitude of Ca(2+)-activated K(+) current at the whole-cell level, occur through allosteric mechanisms. The collaborative interplay between membrane depolarization and heightened intracellular Ca(2+) ion concentrations collectively contribute to the activation of BK(Ca) channels. Although fully developed mammalian cardiac cells do not exhibit functional expression of these ion channels, evidence suggests their presence in cardiac fibroblasts that surround and potentially establish close connections with neighboring cardiac cells. When cardiac cells form close associations with fibroblasts, the high single-ion conductance of these channels, approximately ranging from 150 to 250 pS, can result in the random depolarization of the adjacent cardiac cell membranes. While cardiac fibroblasts are typically electrically non-excitable, their prevalence within heart tissue increases, particularly in the context of aging myocardial infarction or atrial fibrillation. This augmented presence of BK(Ca) channels' conductance holds the potential to amplify the excitability of cardiac cell membranes through effective electrical coupling between fibroblasts and cardiomyocytes. In this scenario, this heightened excitability may contribute to the onset of cardiac arrhythmias. Moreover, it is worth noting that the substances influencing the activity of these BK(Ca) channels might influence cardiac electrical activity as well. Taken together, the BK(Ca) channel activity residing in cardiac fibroblasts may contribute to cardiac electrical function occurring in vivo.